Evidence map›Paper›PMID 32678044›Full record

ArticleRespiratory research2020

In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression.

Hélène Le Ribeuz, Audrey Courboulin, Maria-Rosa Ghigna, Mélanie Lambert, Aurélie Hautefort, Marc Humbert, David Montani, Sylvia Cohen-Kaminsky, Frédéric Perros, Fabrice Antigny

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  4. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 1 institution in 2 countries.

Hélène Le RibeuzFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Audrey CourboulinFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Maria-Rosa GhignaFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Mélanie LambertFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Aurélie HautefortFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Marc HumbertFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
David MontaniFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Sylvia Cohen-KaminskyFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Frédéric PerrosFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France.
Fabrice AntignyFaculté de Médecine, Université Paris-Saclay, Le Kremlin-Bicêtre, France. antignyfabrice@gmail.com.ORCID http://orcid.org/0000-0002-9515-6571
Inserm · FR

Funding

Agence Nationale de la Recherche ANR-18-CE14-0023
6 · The paper itself

Abstract

backgroundThe pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. METHODS AND

resultsMiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs.

conclusionsWe confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression.

Indexed as

Arterial PressureAdministration, InhalationAnimalsAntagomirsCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationHumansMaleMicroRNAsMonocrotalineMonosaccharide Transport ProteinsNerve Tissue ProteinsPotassium Channels, Tandem Pore DomainPulmonary Arterial HypertensionAntagomirsMicroRNAsMIRN138 microRNA, humanMIRN138 microRNA, ratMonocrotalineMonosaccharide Transport ProteinsNerve Tissue ProteinsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3KCNK3miR-138PAHProliferationSLC45A3

Identifiers

PMID32678044
PMCPMC7364627
OpenAlexW3043405990

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.